Acid-base balance and disturbance

Normal acid-base balance

Parameters of acid-base balance

Simple acid-base disturbance

Mixed acid-base disturbance

Normal acid-base balance

Concepts of acid and base

Sources of acids and bases

Regulation of acid-base balance

Concepts of acid and base

H2CO3=H++HCO3-

HHb=H++ Hb-

H2PO4-=H++HPO4

2-

HPr=H++Pr-

Acid base

H+donor H+ receptor

Sources of acids and bases

mainly produced during the catabolism of intracellular nutrients, with a small part of them from food.

Acid

Volatile acid carbonic acid

Nonvolatile acid or fixed acid sulfuric acid, phosphoric acid, lactic acid, acetoacetic acid, β-hydroxybutyric acid

Regulation of acid-base balance

Buffer systems

Respiratory regulation of acid-base balance

Renal regulation of acid-base balance

Buffer systems

Buffer system in the blood

Buffer effect of cells

Buffer system in the blood

H2CO3=H++HCO3-

H2PO4-=H++HPO4

2-

HPr=H++Pr-

HHb=H++Hb-

HHbO2=H++HbO2-

Buffer acid buffer base

Weak acid conjugate base

Converting strong acid or base into weak acid or base

Buffer effect of cells

Ion exchange between intracellular and extracellular fluids

H+ k+

HCO3- Cl-

Intracellular buffer systems

H2PO4-/HPO4

2-

HPr/Pr-

Respiratory regulation of acid-base

Central chemoreceptor

Peripheral chemoreceptor

Respiratory center

ventilation

H+, PaCO2, PaO2H+

Renal regulation of acid-base balance

Excretion of H+ and reabsorption of HCO3- in proximal convoluted tubule

Excretion of H+ and reabsorption of HCO3- in distal tubule

Excretion of NH4+ and NH3

Parameters of acid-base balance

pH 7.35-7.45

H2CO3=H++HCO3-

[H+]=pKa.[H2CO3]/[HCO3-]

[H2CO3]=0.03PaCO2=1.2

PaCO2

PaCO2 is the partial pressure of CO2 dissolved in artery plasma, the normal range is 33-46mmHg with a average value of 40mmHg.

PaCO2 reflects the situation of alveolar ventilation.

PaCO2↑ respiratory acidosis or metabolic alkalosis after compensation

PaCO2↓ respiratory alkalosis or metabolic acidosis after compensation

Standard bicarbonate (SB) and actual bicarbonate (AB)

SB is the bicarbonate under “standard condition” which refers to a temperature of 38 , PaCO2 of ℃40mmHg and 100% oxygen saturation of hemoglobin.

Normal range: 22-27mmol/L

Average value:24mmol/L

SB↑ metabolic alkalosis or chronic respiratory acidosis

SB↓ metabolic acidosis or chronic respiratory alkalosis

AB

AB is the bicarbonate measured under “actual condition” which refers to the actual status of the patient.

A comparison between SB and AB can provide some information for the differentiation of respiratory acid-base disturbance from metabolic acid-base disturbance.

Buffer base (BB)

BB is the sum of all all alkaline buffer substances in the blood, which is also measured under standard condition.

Normal range: 45-52mmol/L

Average value: 48mmol/L

Base excess (B E)

BE describes the amount if a fixed acid or base that must be added to a blood sample to achieve a pH of 7.4 under standard condition.

If an acid must be added, the BE value is positive.

If an base must be added, the BE value is negative.

The normal value is -3-+3mmol/L

Anion gap (AG)

AG is the difference between unmeasured anion (UA) and unmeasured cation (UC).

AG=UA-UC=Na+-(Cl-+HCO3-)=140-104-

24=12mmol/L

AG↑ metabolic acidosis

Simple acid-base disturbance

Metabolic acidosis

respiratory acidosis

Metabolic alkalosis

Respiratory alkalosis

Metabolic acidosis

Metabolic acidosis is defined as a decrease of pH induced by primary decrease in plasma bicarbonate concentration.

etiology

Excessive production of fixed acid

lactic acidosis (glycolysis) keto-acidosis (lipolysis)

Disorders in the excretion of acidic metabolites

renal failure, renal tubular acidosis I

Excessive loss of HCO3-

loss of intestinal juice, bile, and pancreatic juice

renal tubular acidosis II

Excessive intake of exogenous acids

NH4Cl, aspirin (acetylsalicylic acid)

hyperkalemia

Classification

Normal AG metabolic acidosis

loss of HCO3- from intestinal of renal

route

excessive intake of chloride- containing medicine

High AG metabolic acidosis

lactic acidosis, keto-acidosis

renal failure, salicylic poisoning

compensation

Compensation by the buffer system

Compensation by the lung

ventilation↑→PaCO2↓

△PaCO2=1.2 HCO△ 3-±2

Compensation by the kidney

Changes of acid-base parameters

pH ↓, SB ↓, AB ↓, BE ↓PaCO2 ↓ AB<SB

Alterations of metabolism and function

Cardiovascular system

Central nervous system

Cardiovascular system

Cardiac arrhythmia hyperkalemia

Negative inotropic action

H+ can competitively inhibit the combination of Ca2+ with troponin and influence the influx of Ca2+ from extracellular space and the release of Ca2+ into cytoplasm from sarcoplasmic reticulum.

Decreased response of vascular system to CA

Central nervous system

Weakness, fatigue, lethargy, disorder of consciousness, coma

Activities of Glutamate decarboxylase ↑

Gamma-aminobutyric acid (GABA) ↑

Activities of oxygenase in mitochondria ↓

ATP ↓

Correction of underlying disorders

Administration of NaHCO3

Attention should be paid to prevent hypokalemia and convulsion induced by decreased free Ca2+

Principles of prevention and treatmen

Respiratory acidosis

Respiratory acidosis is defined as a decrease of pH induced by primary increase in plasma H2CO3 concentration.

Etiology

Suppression of respiratory center

Cerebrovascular accident

Trauma or infection of brain

Excessive sedatives, narcotics, alcohol

Disease of respiratory muscles

Acute radiculitis

Acute poliomyelitis

Organophosphorus pesticide poisoning

Severe hypokalemia

Disease of chest wall

Pneumothorax, hydrops of thoracic cavity, chest deformity

Obstruction of airways

Drowning

Aspiration of foreign bodies

Laryngeal edema

Laryngospasm

Chronic obstructive pulmonary disease

Pulmonary disease

Extensive inflammation

Consolidation

fibrosis

Excessive inspiration of CO2

compensation

Acute respiratory acidosis

H+-K+ exchange

Buffer effect of red blood cells Cl- -HCO3- exchange

Chronic respiratory acidosis

Kidney excretion of H+ and NH4+↑,reabsorption of HCO3

-↑

△[HCO3-]=0.1 PaCO△ 2±1.5

△[HCO3-]=0.4 PaCO△ 2±3

Changes of acid-base parameters

pH ↓, PaCO2↑ SB ↑, AB ↑, BE ↑ AB>SB

Alterations of metabolism and function

Central nervous system

Cardiovascular system

Nervous system

CO2 narcosis headache, fatigue, mental derangement, tremor, lethargy, coma

Pulmonary encephalopathy hypercapnia and hypoxia

Cardiovascular system

Dilation of brain blood vessels , intracranial hypertension, brain edema

Cardiac arrhythmia and decreased cardiac contractility

Principles of prevention and treatmen

Keep the airway unobstructed and to improve ventilation

Tracheotomy, intratrachea intubation, mechanical ventilation

Metabolic alkalosis

Metabolic alkalosis is defined as a increase of pH induced by primary increase in plasma bicarbonate concentration.

Etiology

Excessive loss of fixed acid

loss from the stomach vomiting, gastric suction

loss from the kidney diuretics, hyperaldosteroism

Excessive intake of alkaline substances

NaHCO3, stored blood (citrate)

Hypokalemia paradoxical acidic urine

Classification

Saline-responsive alkalosis

vomiting, gastric suction, diuretics

Saline-resistant alkalosis

hyperaldosteroism , severe hypokalemia

Compensation

Compensation by the buffer system

Compensation by the lung

ventilation↓→PaCO2↑

△PaCO2=0.7 HCO△ 3-±5

Compensation by the kidney

pH ↑, SB ↑, AB ↑, BE ↑ AB>SB PaCO2↑

Changes of acid-base parameters

Alterations of metabolism and function

Central nervous system

restless, mental derangement, delirium, disorder of consciousness, GABA↓

Oxygen dissociation curve of hemoglobin shifts to left

Free calcium ↓

convulsion, tendon hyperreflexia

hypokalemia

Principles of prevention and treatmen

Saline-responsive alkalosis

NaCl, KCl, CaCl2

Saline-resistant alkalosis

antisterone, potassium, carbonic anhydrase (CA)

Respiratory alkalosis

Respiratory alkalosis is defined as a increase of pH induced by primary decrease in plasma H2CO3 concentration.

Etiology

Psychogenic factors nervousness, anxiety, hysteria

Hypoxemia

Some pulmonary disease ARDS

Brain diseases encephalitis, meningitis

Misuse of mechanical ventilation

Acute respiratory alkalosis

H+-K+ exchange

Buffer effect of red blood cells

Cl- -HCO3- exchange

△[HCO3-]=0.2 PaCO△ 2±2.5

Chronic respiratory alkalosis

Kidney excretion of H+ and NH4+↓,reabsorption of HCO3

-↓

△[HCO3-]=0.5 PaCO△ 2±2.5

Compensation

Changes of acid-base parameters

pH ↑, PaCO2 ↓ ,SB ↓, AB ↓, BE ↓, AB<SB

Alterations of metabolism and function

Disturbance in CNS vertigo, disorder of consciousness, coma

Increased neuromuscular excitability, tetany, convulsion

Principles of prevention and treatmen

Treatment of primary disease

Prevention mechanical hyperventilation

Inspiration of oxygen-containing 5% CO2